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  1. #121
    Kärnfysikern's Avatar
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    I havent read anything about vitamin c and liver/kidney so I cant comment on it realy I think r-ala is the best to protect liver.

    if I find something about liver protection from vitamin c I will let you know bro.

  2. #122
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    hey Daz, check in the steroids forum under milk thistle, i posted a few studies showing that R-lipoic acid and SAMe have been shown to be more effective in some cases for liver protection, however, milk thistle is still good (silymarin)...i personally advocate all three, especially during an oral run...

  3. #123
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    it is a diuretic so it would help to flush things through the kidney thats for sure. but I dont know if kidney or liver damage is done via free radicals. Thats something I have never realy read about if it is then vitamin c would be awsome since in the dosage Im talking about its the best anti oxidant there is.

  4. #124
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    I found this -

    "Ascorbic acid lowers Zinc directly, and it lowers it indirectly by supporting iron uptake, so while higher
    intake of Vitamin C would likely be beneficial for those suffering from some forms of anemia, leukemia,

    left-sided ovarian cysts, or from prostatitis, it could compromise benign prostatic hypertrophy, certain

    liver conditions (hemochromatosis), or more serious kidney disease (renal failure). "

    Not sure exactly what it means but if you can decipher it........

    Also -

    "By lowering manganese, Vitamin C affects glycogen stores in the liver, decreasing the liver's ability

    to store larger amounts. Manganese has some control over the liver's ability to break down estrogen,

    so too much Vitamin C can affect the length of the menstrual cycle and worsen low estrogenic-types

    of PMS. On the other hand, congestive liver disease of the right large liver lobe will benefit from a
    greater intake of Vitamin C by reducing the symptoms of high estrogenic-types of PMS, while at the
    same time reducing the risk of developing estrogen-sensitive types of cancers or (fibroid) tumors

    resulting from a lifelong higher mean average of estrogen. "

    Again, may not apply to us ?!???

    http://www.acu-cell.com/vitc.html

  5. #125
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    Antioxidants that Reduce Free-Radical Damage
    Vitamin C. Vitamin C is a potent antioxidant that is found naturally in many fruits and vegetables. According to Garg et al. (2000), vitamin C has protective effects against liver oxidative damage, particularly when used in combination with vitamin E. Researchers have found inadequate levels of vitamin C in patients with degenerative diseases. Garg et al. (2000) found that supplementation in rats lowered plasma and liver lipid peroxidation, normalized plasma vitamin C levels, and raised vitamin E above normal levels.

    Another more helpfull piece - think that answers liver protection Q from Vit C

    http://www.lef.org/protocols/prtcl-125b.shtml

  6. #126
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    yeah the last thing seems to make it clear. and they are probably not even using a tenth of the dosage Im talking about

    il read the first one in a bit

  7. #127
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    interesting about copper and zink. I always thought vit c increases zink absorbation. Ohh well I take 60-90mg of zink everday anyway I also think he overexagerates the thing about copper. I have never ever heard anyone beeing deficit in copper.

    Il read more about that. thanks for the link bro.

  8. #128
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    amazing that it decreases the livers ability to store glycoen thats a big advantage

  9. #129
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    Yeah I agree with the copper bit - theres so much used in pipes it gets in our waters and therefore how can we be deficient of it ????

  10. #130
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    exactly most of us probably have to much. only during very special conditions do i think copper depletion is a issue. and when it comes to zink. Im guessing most of us supplement with zink anyway. I sure do its very important for my sleep

  11. #131
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    Quote Originally Posted by dazbo
    Antioxidants that Reduce Free-Radical Damage
    Vitamin C. Vitamin C is a potent antioxidant that is found naturally in many fruits and vegetables. According to Garg et al. (2000), vitamin C has protective effects against liver oxidative damage, particularly when used in combination with vitamin E. Researchers have found inadequate levels of vitamin C in patients with degenerative diseases. Garg et al. (2000) found that supplementation in rats lowered plasma and liver lipid peroxidation, normalized plasma vitamin C levels, and raised vitamin E above normal levels.

    Another more helpfull piece - think that answers liver protection Q from Vit C

    http://www.lef.org/protocols/prtcl-125b.shtml
    i'm telling you, you'll see this across the board when it comes to vitamins and minerals...those who are defecient are really the ones who benefit from supplementation...i know it's not a popular belief shared on this thread, but ahh well...

  12. #132
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    I think the right ammount of minerals and vitamins can be the cure for just about anything almost. the foundation of orthomolecular medicin

  13. #133
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    btw alpha here is a good read
    http://www.internetwks.com/owen/heart.htm

    Linus Pauling and your Heart
    (c) 1996 Owen R. Fonorow
    At the age of 93, dual Nobel prize winning scientist Linus Pauling, well known for advocating the healthful benefits of vitamin C, anounced that, "we've got to the point where I think we can get almost complete control of cardiovascular disease, heart attacks and strokes." Now, several years later, as evidence mounts, Linus Pauling's belief is being affirmed.

    A provocative series of papers was published by Dr. G. C. Willis and coworkers starting in 1953 that showed the importance of ascorbic acid in the maintenance of the arterial walls (the intima). Any factor disturbing vitamin C metabolism results in wall injury with subsequent fatlike deposits. In his 1953 paper, Willis concludes that acute or chronic vitamin C deficiency in guinea pigs produces atheroslcerosis and closely simulates the human form of the disease.

    In 1954 the Willis group studied the actual progression of atherosclerotic plaques in living patients by a serial X-ray technique. The study demonstrated a reduction in atherosclerotic plaque lesions in the group of vitamin C patients not observed in the controls. Based on these careful studies, Willis announced that "Massive does of parenteral ascorbic acid (vitamin C) may be of therapeutic value in the treatment of atherosclerosis and the prevention of intimal hemorhage and thrombosis." This announcement was generally ignored by the medical community.

    Recently, another study by Joseph Vita, M.D., an associate professor of medicine at Boston University school of Medicine found that vitamin C improved blood-vessel dilation in patients with coronary artery disease. Vita found that 2000 mg of vitamin C, (which is approximately 30 times the U. S. RDA) open arteries by almost 10% - more than some medical treatments.

    In another recent study, Thomas Heitzer, M.D., and his colleagues at the University of Freiburg, Germany, compared blood flow in the forearm brachial arteries of 10 healthy male non-smokers and 10 male chronic smokers after infusing two chemicals, followed by injections of vitamin C. The study published in the Journal Circulation of the American Heart Association (AHA), showed that vitamin C injected into the blood stream "almost completely reverses endothelial dysfunction in chronic smokers."

    It has been widely recognized for at least a decade that endothelial lesions (damage to the walls of blood vessels) are a necessary precondition for the development of atherosclerotic plaques. Oxidized LDL cholesterol and vitamin deficiencies have been theorized to cause these lesions.

    According to the AHA: Injured endothelial cells may initiate an inflammatory response leading to increased deposits of "bad" cholesterol and other substances in the artery wall -- a process known as atherosclerosis, which can lead to coronary heart disease and heart attack. The author believes that because Vitamin C in the blood stream has been reliably shown to correct this precondition, it can be concluded that Linus Pauling analysis was correct: Vitamin C in the blood stream is preventative against cardiovascular disease (CVD).

    During the 1970s, Vitamin C consumption in the U.S. rose by 300%. Mortality from heart disease decreased by 30%. The U.S. was the only country during this time frame with a significant drop in heart disease fatalities. In 1992 Dr. Enstrom and colleagues (UCLA) showed (in over 11,000 people) that increased intake of vitamin C reduces the death rate from heart disease by nearly half and prolongs life for more than six years.

    The most recent report from the British Medical Journal reported on a study of 1,605 randomly selected men in Finland, aged 42 to 60 years. The study was conducted between 1984 and 1989. None of the men had evidence of pre-existing heart disease. After adjusting for other confounding factors, men who were deficient in vitamin C had 3.5 times more heart attacks then men who were not deficient in vitamin C. The scientists' conclusion was, "Vitamin C deficiency, as assessed by low plasma ascorbate concentration, is a risk factor for coronary heart disease." British Medical Journal (Vol 314, Issue 708, 1997).

    LIPOPROTEIN(a)
    There is a strange variant of the well known LDL (bad) cholesterol in the blood of human beings. This LDL look-alike is not present in the blood of most animals. Dr. Matthias Rath, M.D. was a member of the German team that discovered this substance, called Lipoprotein(a) (Lp(a)), is the primary constituent of plaque in post-mortem human aortas. A finding recently verified at Baylor University Medical School, according to Dr. Rath.
    Dr. Pauling suggests that Lp(a), rather than LDL cholesterol, is the real danger to human health. Levels of Lp(a) in the blood are associated with the level of vitamin C in the body. Recently, a study published in the August 21, 1996 Journal of the American Medical Association again confirmed that Lp(a) is an independent risk factor in cardiovascular disease. Since 1994, some 986 Lp(a) studies have implicated the highly atherogenic Lp(a) as a risk factor.

    LP(a) A SURROGATE FOR VITAMIN C
    The Pauling/Rath theory of heart disease claims that Lp(a), with its "sticky" surface that makes it adhere to damaged blood vessels, acts as a surrogate for chronic low levels of vitamin C in human beings. Pauling claims that heart disease begins when there is not sufficient Vitamin C to support collagen synthesis. Both vitamin C and Lp(a) promote the "structural integrity" of blood vessels. When collagen synthesis is inadequate due to lack of vitamin C, Lp(a) "repairs" the areas of deficiency -- somewhat like a "plaster cast." This healing process forms what are known as plaques.
    Coronary arteries are squeezed by the heartbeat. Rath likens the stress to that of stepping on a garden hose thousands of times every day, day in and day out. Coronary arteries lacking collagen and elastin due to chronic vitamin C deficiency are more susceptible to damage from this kind of stress. If blood vessels that are kept strong by an optimum intake of vitamin C,(and other antioxidants), lesions will not develop. If lesions do not develop, according to theory, heart disease does not develop.

    According to Nobel prize winning physicist Richard Feynman:

    "The principle of science, the definition, almost, is the following: The test of all knowledge is experiment. Experiment is the sole judge of scientific "truth."
    Most animals produce their own vitamin C, and according to Pauling, do not have Lp(a) in their blood. However, guinea pigs, like humans, do not produce their own vitamin C. If these animals a deprived of all vitamin C they die a horrible death in two weeks. Pauling and Rath wondered whether they also produce Lp(a) like we humans. An experiment to test theory was conducted at the Linus Pauling Institute of Science and Medicine.

    Laboratory guinea pigs were divided into two groups. One group, all who were given small amounts of vitamin C (roughly equivalent to the U. S. RDA) Lp(a) was detected and as levels rose over the course of their lifetimes the animals developed atherosclerosis. The pathology of the disease is equivalent with human atherosclerosis.

    Animals in the other group (on the same diet) were given the human equivalent of 3000-5000 mgs/day of vitamin C. These animals did not develop the disease and Lp(a) levels remained low. The only difference between the two groups was the vitamin C. Too little vitamin C made all the difference. This experimental work (confirming the earlier findings by Willis) lead to the first U.S. patent for reversing heart disease without surgery in 1994.

    Competing theories must be able to explain why heart disease does not occur in animals, and why atherosclerotic plaques form mostly in areas of high mechanical stress, rather than randomly throughout the body.

    L-LYSINE
    The key to a possible "non surgical" cure for heart disease came when highly regarded biochemists and chemists discovered that the amino acid, lysine, is contained in a protein in artery walls. Lysine residues are exposed when the arterial wall is damaged. L-lysine is one of the twenty essential amino acids, and lipoprotein-(a) binds to it.
    Said Pauling, "knowing that lysyl residues are what causes lipoprotein-(a) to get stuck to the wall of the artery and form atherosclerotic plaques, any physical chemist would say at once that the thing to do is prevent that by putting the amino acid lysine in the blood to a greater extent than it is normally."


    "You need lysine to be alive, is is essential, you have to get about 1 gram a day to keep in protein balance, but you can take lysine, pure lysine, a perfectly non toxic substance in food [as supplements], and that puts extra lysine molecules in the blood. They enter into competition with the lysyl residues on the wall of arteries and accordingly count to prevent Lp(a) from being deposited or even will work to pull it loose and destroy atherosclerotic plaques."
    Pauling filmed a video tape of his lecture on Heart Disease at the age of 92 shortly before his death. On this video Pauling cites three cases were a vitamin C and l-lysine treatment worked miraculously. I know the patient in the following case. Before and after surgery verified the efficacy of the vitamin C and l-lysine treatment.

    Rich B. of Shorewood Illinois had a routine physical exam recently. His doctor discovered blockage in both of his Carotid arteries. Ultrasound showed 90% on one side; 50-60% on the other. Two operations were scheduled. In May 1996 the expected 90% blockage was found and the white plaque removed and the doctor showed it to Rich and his wife. The second operation was scheduled for a month later in June. Rich's wife Betty, was able to convince Rich after the first operation to follow Pauling's recommendations, i.e., to take both vitamin C and the essential amino acid L-lysine. He consumed approximately 1/2 of Linus Pauling's recommended dosage of both vitamin C and L-lysine (or 2500 mg of each) every day for that month. Rich's second operation was performed in June. His doctors were astounded. While the first operation showed no bruises, Rich is bruised from the second up and down his neck; they couldn't find a blockage they knew "had to be there." His carotid arteries had apparently cleared! (Betty and Rich never mentioned the vitamin C/Lysine therapy to their doctor, but we have since written to him asking for copies of the relevant medical records, and permission to use them on the internet.)

    Rich's case of a few weeks ago is telling. Linus Pauling himself reported similar experience in periods as short as 2-4 weeks. More and more reports attest to the pronounced effect of this treatment, especially on patients with severe disease.

    When Pauling was asked if he really thought this development represented the cure for heart disease, he responded:

    "I think so. Yes. Now Ive got to the point where I think we can get almost complete control of cardiovascular disease, heart attacks and strokes by the proper use of vitamin C and Lysine. It can prevent cardiovascular disease and even cure it. If you are at risk of heart disease, or if there is a history of heart disease in your family, if your father or other members of the family died of a heart attack or stroke or whatever, or if you have a mild heart attack yourself then you had better be taking vitamin C and Lysine."
    Linus Pauling's one hour lecture is now available on VHS video from the Life Extension Foundation. 1-800-544-4440.


    OWEN R FONOROW
    PO Box 3097
    Lisle, IL 60532

  14. #134
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    a few comments, good stuff though...

    Quote Originally Posted by johan
    btw alpha here is a good read
    http://www.internetwks.com/owen/heart.htm

    Linus Pauling and your Heart
    (c) 1996 Owen R. Fonorow
    At the age of 93, dual Nobel prize winning scientist Linus Pauling, well known for advocating the healthful benefits of vitamin C, anounced that, "we've got to the point where I think we can get almost complete control of cardiovascular disease, heart attacks and strokes." Now, several years later, as evidence mounts, Linus Pauling's belief is being affirmed.

    A provocative series of papers was published by Dr. G. C. Willis and coworkers starting in 1953 that showed the importance of ascorbic acid in the maintenance of the arterial walls (the intima). Any factor disturbing vitamin C metabolism results in wall injury with subsequent fatlike deposits. In his 1953 paper, Willis concludes that acute or chronic vitamin C deficiency in guinea pigs produces atheroslcerosis and closely simulates the human form of the disease.

    In 1954 the Willis group studied the actual progression of atherosclerotic plaques in living patients by a serial X-ray technique. The study demonstrated a reduction in atherosclerotic plaque lesions in the group of vitamin C patients not observed in the controls. Based on these careful studies, Willis announced that "Massive does of parenteral ascorbic acid (vitamin C) may be of therapeutic value in the treatment of atherosclerosis and the prevention of intimal hemorhage and thrombosis." This announcement was generally ignored by the medical community. WHAT GAVE THEM THE ATHEROSCLEROSIS IN THE FIRST PLACE? IMPROPER NUTRITION PROBABLY, WHICH IS LACKING IN ALL VITAMINS

    Recently, another study by Joseph Vita, M.D., an associate professor of medicine at Boston University school of Medicine found that vitamin C improved blood-vessel dilation in patients with coronary artery disease. Vita found that 2000 mg of vitamin C, (which is approximately 30 times the U. S. RDA) open arteries by almost 10% - more than some medical treatments. PROBABLY SHITTY DIETS HERE TOO.

    In another recent study, Thomas Heitzer, M.D., and his colleagues at the University of Freiburg, Germany, compared blood flow in the forearm brachial arteries of 10 healthy male non-smokers and 10 male chronic smokers after infusing two chemicals, followed by injections of vitamin C. The study published in the Journal Circulation of the American Heart Association (AHA), showed that vitamin C injected into the blood stream "almost completely reverses endothelial dysfunction in chronic smokers." NO NEED TO COMMENT HERE.

    It has been widely recognized for at least a decade that endothelial lesions (damage to the walls of blood vessels) are a necessary precondition for the development of atherosclerotic plaques. Oxidized LDL cholesterol and vitamin deficiencies have been theorized to cause these lesions.

    According to the AHA: Injured endothelial cells may initiate an inflammatory response leading to increased deposits of "bad" cholesterol and other substances in the artery wall -- a process known as atherosclerosis, which can lead to coronary heart disease and heart attack. The author believes that because Vitamin C in the blood stream has been reliably shown to correct this precondition, it can be concluded that Linus Pauling analysis was correct: Vitamin C in the blood stream is preventative against cardiovascular disease (CVD). SURE, BUT AT WHAT LEVELS? AGAIN, PROPER NUTRITION WOULD SUFFICE.

    During the 1970s, Vitamin C consumption in the U.S. rose by 300%. Mortality from heart disease decreased by 30%. The U.S. was the only country during this time frame with a significant drop in heart disease fatalities. In 1992 Dr. Enstrom and colleagues (UCLA) showed (in over 11,000 people) that increased intake of vitamin C reduces the death rate from heart disease by nearly half and prolongs life for more than six years. SURELY YOU CAN'T THINK THIS THE ONLY CAUSE...WHAT ABOUT THE OVERALL GREATER ATTENTION TO HEALTHY DIETS/LIFESTYLES OVER THE YEARS?

    The most recent report from the British Medical Journal reported on a study of 1,605 randomly selected men in Finland, aged 42 to 60 years. The study was conducted between 1984 and 1989. None of the men had evidence of pre-existing heart disease. After adjusting for other confounding factors, men who were deficient in vitamin C had 3.5 times more heart attacks then men who were not deficient in vitamin C. The scientists' conclusion was, "Vitamin C deficiency, as assessed by low plasma ascorbate concentration, is a risk factor for coronary heart disease." British Medical Journal (Vol 314, Issue 708, 1997).

    LIPOPROTEIN(a)
    There is a strange variant of the well known LDL (bad) cholesterol in the blood of human beings. This LDL look-alike is not present in the blood of most animals. Dr. Matthias Rath, M.D. was a member of the German team that discovered this substance, called Lipoprotein(a) (Lp(a)), is the primary constituent of plaque in post-mortem human aortas. A finding recently verified at Baylor University Medical School, according to Dr. Rath.
    Dr. Pauling suggests that Lp(a), rather than LDL cholesterol, is the real danger to human health. Levels of Lp(a) in the blood are associated with the level of vitamin C in the body. Recently, a study published in the August 21, 1996 Journal of the American Medical Association again confirmed that Lp(a) is an independent risk factor in cardiovascular disease. Since 1994, some 986 Lp(a) studies have implicated the highly atherogenic Lp(a) as a risk factor.

    LP(a) A SURROGATE FOR VITAMIN C
    The Pauling/Rath theory of heart disease claims that Lp(a), with its "sticky" surface that makes it adhere to damaged blood vessels, acts as a surrogate for chronic low levels of vitamin C in human beings. Pauling claims that heart disease begins when there is not sufficient Vitamin C to support collagen synthesis. Both vitamin C and Lp(a) promote the "structural integrity" of blood vessels. When collagen synthesis is inadequate due to lack of vitamin C, Lp(a) "repairs" the areas of deficiency -- somewhat like a "plaster cast." This healing process forms what are known as plaques.
    Coronary arteries are squeezed by the heartbeat. Rath likens the stress to that of stepping on a garden hose thousands of times every day, day in and day out. Coronary arteries lacking collagen and elastin due to chronic vitamin C deficiency are more susceptible to damage from this kind of stress. If blood vessels that are kept strong by an optimum intake of vitamin C,(and other antioxidants), lesions will not develop. If lesions do not develop, according to theory, heart disease does not develop.

    According to Nobel prize winning physicist Richard Feynman:

    "The principle of science, the definition, almost, is the following: The test of all knowledge is experiment. Experiment is the sole judge of scientific "truth."
    Most animals produce their own vitamin C, and according to Pauling, do not have Lp(a) in their blood. However, guinea pigs, like humans, do not produce their own vitamin C. If these animals a deprived of all vitamin C they die a horrible death in two weeks. Pauling and Rath wondered whether they also produce Lp(a) like we humans. An experiment to test theory was conducted at the Linus Pauling Institute of Science and Medicine.

    Laboratory guinea pigs were divided into two groups. One group, all who were given small amounts of vitamin C (roughly equivalent to the U. S. RDA) Lp(a) was detected and as levels rose over the course of their lifetimes the animals developed atherosclerosis. The pathology of the disease is equivalent with human atherosclerosis. NOW THIS MAY BE YOUR BEST CASE YET, BUT I'D LIKE TO REVIEW THE ENTIRE STUDY IF YOU HAVE REFERENCE TO IT.

    Animals in the other group (on the same diet) were given the human equivalent of 3000-5000 mgs/day of vitamin C. These animals did not develop the disease and Lp(a) levels remained low. The only difference between the two groups was the vitamin C. Too little vitamin C made all the difference. This experimental work (confirming the earlier findings by Willis) lead to the first U.S. patent for reversing heart disease without surgery in 1994. BUT HERE, IT DOESN'T REALLY TAKE INTO ACCOUNT ANY OTHER FACTORS, LIFESTYLE, EXERCISE, OVERALL EATING HABITS

    Competing theories must be able to explain why heart disease does not occur in animals (PROBABLY BECAUSE THEY DON'T SMOKE OR EAT ALL THE PROCESSED CRAP AND FATS THAT WE DO), and why atherosclerotic plaques form mostly in areas of high mechanical stress, rather than randomly throughout the body.

    L-LYSINE
    The key to a possible "non surgical" cure for heart disease came when highly regarded biochemists and chemists discovered that the amino acid, lysine, is contained in a protein in artery walls. Lysine residues are exposed when the arterial wall is damaged. L-lysine is one of the twenty essential amino acids, and lipoprotein-(a) binds to it.
    Said Pauling, "knowing that lysyl residues are what causes lipoprotein-(a) to get stuck to the wall of the artery and form atherosclerotic plaques, any physical chemist would say at once that the thing to do is prevent that by putting the amino acid lysine in the blood to a greater extent than it is normally."


    "You need lysine to be alive, is is essential, you have to get about 1 gram a day to keep in protein balance, but you can take lysine, pure lysine, a perfectly non toxic substance in food [as supplements], and that puts extra lysine molecules in the blood. They enter into competition with the lysyl residues on the wall of arteries and accordingly count to prevent Lp(a) from being deposited or even will work to pull it loose and destroy atherosclerotic plaques." BUT WITH A HIGH PROTEIN DIET AND A GOOD MULTI, DONT YOU THINK YOU CAN ACHIEVE THE SAME?
    Pauling filmed a video tape of his lecture on Heart Disease at the age of 92 shortly before his death. On this video Pauling cites three cases were a vitamin C and l-lysine treatment worked miraculously. I know the patient in the following case. Before and after surgery verified the efficacy of the vitamin C and l-lysine treatment.

    Rich B. of Shorewood Illinois had a routine physical exam recently. His doctor discovered blockage in both of his Carotid arteries. Ultrasound showed 90% on one side; 50-60% on the other. Two operations were scheduled. In May 1996 the expected 90% blockage was found and the white plaque removed and the doctor showed it to Rich and his wife. The second operation was scheduled for a month later in June. Rich's wife Betty, was able to convince Rich after the first operation to follow Pauling's recommendations, i.e., to take both vitamin C and the essential amino acid L-lysine. He consumed approximately 1/2 of Linus Pauling's recommended dosage of both vitamin C and L-lysine (or 2500 mg of each) every day for that month. Rich's second operation was performed in June. His doctors were astounded. While the first operation showed no bruises, Rich is bruised from the second up and down his neck; they couldn't find a blockage they knew "had to be there." His carotid arteries had apparently cleared! (Betty and Rich never mentioned the vitamin C/Lysine therapy to their doctor, but we have since written to him asking for copies of the relevant medical records, and permission to use them on the internet.) I'D HAVE TO KNOW MORE ABOUT THIS GUY TO PROPERLY ASSESS THIS...DOESNT SEEM LIKE THEY WERE ABLE TO PROVIDE A DIRECT LINK HERE.

    Rich's case of a few weeks ago is telling. Linus Pauling himself reported similar experience in periods as short as 2-4 weeks. More and more reports attest to the pronounced effect of this treatment, especially on patients with severe disease.

    When Pauling was asked if he really thought this development represented the cure for heart disease, he responded:

    "I think so. Yes. Now Ive got to the point where I think we can get almost complete control of cardiovascular disease, heart attacks and strokes by the proper use of vitamin C and Lysine. It can prevent cardiovascular disease and even cure it. If you are at risk of heart disease, or if there is a history of heart disease in your family, if your father or other members of the family died of a heart attack or stroke or whatever, or if you have a mild heart attack yourself then you had better be taking vitamin C and Lysine." DOESNT REALLY TELL YOU HOW MUCH THOUGH...
    Linus Pauling's one hour lecture is now available on VHS video from the Life Extension Foundation. 1-800-544-4440.


    OWEN R FONOROW
    PO Box 3097
    Lisle, IL 60532
    thanks for the info...see bold/caps

  15. #135
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    cant asnwere any of your questons since I havent started to research vitamin c and the heart yet.

    btw is lp(a) the same as oxidized ldl? if it is I have seen lots of studies that shows that vitamin c prevents ldl from oxidizing

  16. #136
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    found 2 studies now that shows ascorbic acid doesnt lower lp(a). Will keep on digging

  17. #137
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  18. #138
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    hiv and ascorbic acid
    http://www.ncbi.nlm.nih.gov/entrez/q...293&query_hl=1

    Suppression of human immunodeficiency virus replication by ascorbate in chronically and acutely infected cells.

    Harakeh S, Jariwalla RJ, Pauling L.

    Viral Carcinogenesis, Laboratory, Linus Pauling Institute of Science and Medicine, Palo Alto, CA 94306.

    We have studied the action of ascorbate (vitamin C) on human immunodeficiency virus type 1 (HIV-1), the etiological agent clinically associated with AIDS. We report the suppression of virus production and cell fusion in HIV-infected T-lymphocytic cell lines grown in the presence of nontoxic concentrations of ascorbate. In chronically infected cells expressing HIV at peak levels, ascorbate reduced the levels of extracellular reverse transcriptase (RT) activity (by greater than 99%) and of p24 antigen (by 90%) in the culture supernatant. Under similar conditions, no detectable inhibitory effects on cell viability, host metabolic activity, and protein synthesis were observed. In freshly infected CD4+ cells, ascorbate inhibited the formation of giant-cell syncytia (by approximately 93%). Exposure of cell-free virus to ascorbate at 37 degrees C for 1 day had no effect on its RT activity or syncytium-forming ability. Prolonged exposure of virus (37 degrees C for 4 days) in the presence of ascorbate (100-150 micrograms/ml) resulted in the drop by a factor of 3-14 in RT activity as compared to a reduction by a factor of 25-172 in extracellular RT released from chronically infected cells. These results indicate that ascorbate mediates an anti-HIV effect by diminishing viral protein production in infected cells and RT stability in extracellular virions.

    PMID: 1698293 [PubMed - indexed for MEDLINE]

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    this one shows lowering effect on lp(a) in guine pig

    Immunological evidence for the accumulation of lipoprotein(a) in the atherosclerotic lesion of the hypoascorbemic guinea pig.

    Rath M, Pauling L.

    Linus Pauling Institute of Science and Medicine, Palo Alto, CA 94306-2025.

    Lipoprotein(a) [Lp(a)] is an extremely atherogenic lipoprotein. Lp(a) has been found in the plasma of humans and other primates, but until now only in a few other species. The mechanism by which it exerts its atherogenicity is still poorly understood. We observed that Lp(a) has been found in the plasma of several species unable to synthesize ascorbate and not in other species. We have now detected apoprotein(a) in the plasma of the guinea pig. We induced atherosclerosis in this animal by dietary ascorbate depletion and, using SDS/PAGE and subsequent immunoblotting, we identified Lp(a) as accumulating in the atherosclerotic plaque. Most importantly, adequate amounts of ascorbate (40 mg per kg of body weight per day) prevent the development of atherosclerotic lesions in this animal model and the accumulation of Lp(a) in the arterial wall. We suggest an analogous mechanism in humans because of the similarity between guinea pigs and humans with respect to both the lack of endogenous ascorbate production and the role of Lp(a) in human atherosclerosis.

    PMID: 2147514 [PubMed - indexed for MEDLINE]
    to bad that it doesnt seem to carry over to humans. Maby the human studies where low in lysin. Or maby it just doesnt work that way in humans. But there have to be more to it. Linus Pauling would make such a big statement if he wasnt very sure about this word.

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    Now I realise Im reading things to fast. Pauling claims that vitamin c is important for arterie strenght but lysin is the thing that "mops" upp the lp(a). So the studies showing that lp(a) doesnt decrease with vitamin c doesnt prove pauling wrong.

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    http://www.ncbi.nlm.nih.gov/entrez/q..._uids=12875759

    Vitamin C and risk of coronary heart disease in women.

    Osganian SK, Stampfer MJ, Rimm E, Spiegelman D, Hu FB, Manson JE, Willett WC.

    Department of Medicine, Children's Hospital, Boston, Massachusetts, USA. stavroula.osganian@TCH.harvard.edu

    OBJECTIVES: Our objective was to prospectively examine the relation between vitamin C intake and risk of coronary heart disease (CHD) in women. BACKGROUND: Results from prospective investigations of the relation between vitamin C intake and risk of CHD have been inconsistent. The lack of clear evidence for a protective association despite a plausible mechanism indicates the need to evaluate further the association between vitamin C intake and risk of CHD. METHODS: In 1980, 85,118 female nurses completed a detailed semiquantitative food-frequency questionnaire that assessed their consumption of vitamin C and other nutrients. Nurses were followed up for 16 years for the development of incident CHD (nonfatal myocardial infarction and fatal CHD). RESULTS: During 16 years of follow-up (1,240,566 person-years), we identified 1,356 incident cases of CHD. After adjustment for age, smoking, and a variety of other coronary risk factors, we observed a modest significant inverse association between total intake of vitamin C and risk of CHD (relative risk [RR] = 0.73; 95% confidence interval [CI] 0.57 to 0.94). Among women who did not use vitamin C supplements or multivitamins, the association between intake of vitamin C from diet alone and incidence of CHD was weak and not significant (RR = 0.86; 95% CI 0.59 to 1.26). In multivariate models adjusting for age, smoking, and a variety of other coronary risk factors, vitamin C supplement use was associated with a significantly lower risk of CHD (RR = 0.72; 95% CI 0.61 to 0.86). CONCLUSIONS: Users of vitamin C supplements appear to be at lower risk for CHD.

    PMID: 12875759 [PubMed - indexed for MEDLINE]

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    the one above and this one only deals with the dangers of low vit c so not that related to thread but still a good read

    Antioxidant vitamins and mortality in older persons: findings from the nutrition add-on study to the Medical Research Council Trial of Assessment and Management of Older People in the Community.

    Fletcher AE, Breeze E, Shetty PS.

    Centre for Ageing and Public Health, London School of Hygiene and Tropical Medicine, United Kingdom. astrid.fletcher@lshtm.ac.uk

    BACKGROUND: Older persons are at risk of both poor nutrition and increased oxidative stress. Plasma ascorbate concentrations fall with increasing age, and concentrations of other antioxidants may also be reduced. OBJECTIVE: The goal was to examine the association between antioxidants and mortality in older persons. DESIGN: We randomly selected persons aged 75-84 y from the lists of 51 British family practitioners taking part in a randomized trial of assessment of older persons. A total of 1214 participants provided a blood sample and were interviewed about their usual diet with the use of a food-frequency questionnaire. Statistical analyses were based on deaths after a median of 4.4 y of follow-up, and hazard ratios were estimated for quintiles of dietary or blood antioxidants. RESULTS: We found strong inverse trends for blood ascorbate concentrations with all-cause and cardiovascular disease mortality, which were only marginally reduced after adjustment for confounders or supplement use. Those in the lowest fifth (< 17 micromol/L) had the highest mortality, whereas those in the highest fifth (> 66 micromol/L) had a mortality risk nearly half that (hazard ratio = 0.54; 95% CI: 0.34, 0.84). Similar results were found after the exclusion of those subjects with cardiovascular disease or cancer at baseline (hazard ratio = 0.51; 0.28, 0.93). In fully adjusted models, there was no evidence for an influence of alpha-tocopherol, beta-carotene, or retinol on total mortality. Dietary antioxidants measured by the food-frequency questionnaire were not associated with all-cause or cardiovascular disease mortality. CONCLUSION: Low blood vitamin C concentrations in the older British population are strongly predictive of mortality.

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    http://www.ncbi.nlm.nih.gov/entrez/q...st_uids=881295

    Effect of ascorbic acid on plasma cholesterol in humans in a long-term experiment.

    Ginter E, Cerna O, Budlovsky J, Balaz V, Hruba F, Roch V, Sasko E.

    During the period of a low vitamin C intake (approximately equal to 20 mg per day) ascorbic acid in a dose of 2 x 500 mg per day was administered to 82 men and women aged 50-75 years. A correlation of plasma cholesterol levels determined before and after a three months' administration of ascorbic acid showed the effect of vitamin C to be dependent on the starting concentration of plasma cholesterol: the higher the initial cholesterolemia, the greater the hypocholesterolemic effect of ascorbic acid. On restricting the experimental group to subjects with an initial cholesterolemia above 230 mg%, the effect of the same dose of ascorbic acid on cholesterolemia was followed in three-month periods for a further 9 months. In all these time intervals, ascorbic acid was found significantly to depress cholesterolemia and its effects persisted 6 weeks after termination of the experiment. The administration of 2 x 500 mg ascorbic acid daily during one year resulted in an abrupt increase of ascorbemia and a marked accumulation of ascorbic acid in the leucocytes. Six weeks following interruption of ascorbic acid intake, vitamin C concentration in the leucocytes significantly declined but still continued to be twice higher than in the control receiving no ascorbic acid supplement.

    PMID: 881295 [PubMed - indexed for MEDLINE]

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    Improvement of peripheral endothelial dysfunction by acute vitamin C application: different effects in patients with coronary artery disease, ischemic, and dilated cardiomyopathy.

    Erbs S, Gielen S, Linke A, Mobius-Winkler S, Adams V, Baither Y, Schuler G, Hambrecht R.

    University of Leipzig, Heart Center, Department of Internal Medicine/Cardiology, Leipzig, Germany.

    BACKGROUND: Endothelial dysfunction has been described in patients with coronary artery disease (CAD) or chronic heart failure (CHF). Vitamin C administration leads to an improvement of endothelial function by reducing elevated levels of reactive oxygen species. It remains unclear, however, whether the degree of endothelial dysfunction caused by oxidative stress differs between CAD and CHF because of ischemic (ICM) or dilated cardiomyopathy (DCM). METHODS: In patients with CAD (n = 9; left ventricular ejection fraction [LVEF], 64% +/- 3%), ICM (n = 9; LVEF, 25% +/- 4%), DCM (n = 9; LVEF, 25% +/- 3%), and healthy subjects (HS; n = 5; LVEF, 66% +/- 5%) a change in internal radial artery diameter in response to acetylcholine (Ach; 15 and 30 microg/min) was measured with high-resolution ultrasound scanning during a co-infusion of normal saline or vitamin C (25 mg/min). RESULTS: Ach-mediated vasodilation was blunted in patients with CHF (DCM, 90 +/- 20 microm; ICM, 86 +/- 20 microm) and patients with CAD (336 +/- 20 microm) as compared with HS (496 +/- 43 microm; P <.05 vs patients with DCM, ICM, CAD). Vitamin C co-infusion increased Ach-mediated vasodilation by 180 +/- 35 microm (to 270 +/- 30 microm) in DCM (P <.05 vs CAD, HS) and by 294 +/- 40 microm (to 380 +/- 20 microm) in ICM (P <.05 vs DCM, CAD, HS). In patients with CAD, vitamin C increased Ach-mediated vasodilation by 146 +/- 35 microm to normal values, whereas vascular diameter remained unchanged in HS (14 +/- 20 microm; P = not significant). CONCLUSIONS: Acute vitamin C administration restored peripheral endothelial function in patients with CAD to normal values, whereas endothelial function remained attenuated in CHF, in particular in patients with DCM. These results suggest that in patients with CHF, factors other than oxidative stress (eg, cytokines) contribute to the pathologic endothelial function.

    Publication Types:
    Clinical Trial

    PMID: 12891196 [PubMed - indexed for MEDLINE]

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    shouldnt this be good for training? Increasing blod flow?

    Is vitamin C superior to diltiazem for radial artery vasodilation in patients awaiting coronary artery bypass grafting?

    Drossos GE, Toumpoulis IK, Katritsis DG, Ioannidis JP, Kontogiorgi P, Svarna E, Anagnostopoulos CE.

    Department of Cardiothoracic Surgery, University of Ioannina School of Medicine, Ioannina, Greece.

    OBJECTIVES: We aimed to measure the vasodilating effects of vitamin C on the radial arteries of healthy subjects and to assess whether vitamin C is superior in this regard to diltiazem, a commonly used vasodilator in coronary artery bypass using radial conduits. METHODS: In a case-control study (study 1) oral single-dose vitamin C (2 g) was given to 15 healthy nonsmokers and 15 matched otherwise healthy smokers. In a randomized double-blind study (study 2) oral single-dose vitamin C (2 g, n = 15) and diltiazem (180 mg, n = 15) were compared in preoperative patients with coronary artery disease. We examined the dilation of the radial artery with high-resolution ultrasonography and measurement of the lumen surface and color Doppler images of the nondominant radial artery just before and 2 hours after drug administration. RESULTS: In study 1 both smokers and nonsmokers showed a significant increase in the lumen surface at 2 hours compared with at baseline (P <.001 and P =.013, respectively). The increase was larger in smokers (median, 37.5% vs 14.3%; P =.004). In study 2 both groups showed statistically significant increases in the lumen surface at 2 hours compared with at baseline (P <.001 and P =.008 for vitamin C and diltiazem, respectively). Vitamin C achieved a larger increase than diltiazem (median, 33.3% vs 18.2%; P =.016). In multivariate modeling the increase in lumen surface was independently predicted by use of vitamin C over diltiazem (+21.2%, P =.007), diabetes mellitus (+14.5%, P =.085), increased cholesterol (+26.2%, P =.001), and smoking history (+20.8%, P =.017). CONCLUSIONS: Vitamin C is a potent acute vasodilator in both smokers and nonsmokers and is superior to diltiazem in preoperative coronary patients who need protection from vasospasm of the radial conduit.

    Publication Types:
    Clinical Trial
    Randomized Controlled Trial

    PMID: 12579102 [PubMed - indexed for MEDLINE]

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    interesting the vitamin c foundation tried to get a grant to research the effect of lysin along with vitamin c on heart disease. They got denied!!

    Lowering Lp(a) with Ascorbate, Lysine and Proline.
    Our Grant Application to Study Pauling Therapy for Heart Disease that was submitted to the Federal NIH National Center for Complimentary and Alternative Medicine... DENIED!!


    Linus Pauling filmed the video Heart Disease: A Unified Theory of Cause and Treatment to tell the world that ultra high doses of ascorbate (Vitamin C) and lysine should be used to treat heart patients.
    For patients following the advice of their cardiologists, and not supplementing vitamin C, the Pauling Therapy is a miracle.

    In 1993, Pauling recommended not waiting for a time-consuming expensive double-blind study because the potential benefits so far out weigh the risks. Was Pauling right? . Does it really matter? There are no known harmful side effects.

    As of this date, medicine has ignored Pauling and has still not run a double-blind controlled trial!

    Millions more may die if the medical profession does not get with it. See http://www.PaulingTherapy.com for Detailed Information on the nature and cure for Heart Disease.

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    here are a collection of OLD studies about vitamin c and heart diseases. Havent read them yet but I will

    http://vitamincfoundation.org/pdfs/

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    http://www.medical-library.net/sites...r_disease.html

    now Im off to beed. Hope you have some reading alpha. Will be gone the weekend. Spending time with my girl. Wont check the board that much then.

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    Rationale for Use of Massive Doses of Ascorbate in Disease
    Robert F. Cathcart, M.D.
    An ascorbic acid molecule carries two extra electrons with which it can can neutralize two free radicals. When it gives up those two electrons, it is mostly finished unless the mitochondria give it back two electrons. Then the ascorbate can be used over and over again. A major problem, however, is that when there is an inflammation in a tissue, the mitochondria there are so damaged as to not be able to rereduce the dehydroascorbate back to ascorbate. Additionally, the damaged mitochondria become a major source of free radicals. A free radical cascade results.

    Only massive doses of ascorbate will shut down this free radical cascade. I am actually after the extra electrons carried by the ascorbate, not the ascorbate itself. When the concentration of these electrons is raised over a threshold point in the inflamed tissues, the free radicals are instantly neutralized and the free radical cascade is shut down.

    If the concentration of the ascorbate (electrons, reducing redox potential) are driven in high enough concentrations into the inflamed tissues, the inflammation medicated by free radicals, the inflammation will be shut down. Therefore, the degree to which massive doses of ascorbate can cure or ameliorate a condition is proportional to the importance of free radicals in the pathology of that condition.

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    http://www.tomlevymd.com/vcfour.htm

    CHAPTER 4


    THE SAFETY OF HIGH DOSES

    "Opinions are caught like an infection, and
    put into practice without examination."

    Balzac


    Overview


    Along with its numerous and substantial clinical benefits, vitamin C is also one of the safest and least toxic therapies that can be administered to a patient, regardless of diagnosis. Everybody needs some vitamin C on a regular basis, and the only potential problems with vitamin C administration arise in a very limited number of clinical situations. Some researchers have voiced their concerns about the proper dosing of vitamin C in these situations, and the validity of these concerns will be addressed in some detail.


    Long-Term and High-Dose Supplementation


    Intravenous vitamin C has already been demonstrated as a very safe form of vitamin C supplementation. Casciari et al. (2001) reported that "terminal cancer patients" were given 50,000 mg of intravenous vitamin C daily for up to eight weeks. The "blood count and chemistry parameters" revealed no evidence of toxicity or side effects from this administration. Kalokerinos et al. (1982) also reported on the safety of intravenous vitamin C, noting that "in Australia alone, some 100 physicians" have administered as much as 300,000 mg of vitamin C per day to their patients. These authors go on to mention that "in most cases the results have been spectacular, the only side effect is 'chronic good health.'"


    Cathcart (1981), using his method of dosing patients with vitamin C up to "bowel tolerance" (see Chapter 3, in the treatment of AIDS), often gave individual patients more than 200,000 mg of oral vitamin C daily as ascorbic acid. Cathcart (1985) asserted that he had treated over 11,000 patients in the prior 14 years with vitamin C. Regarding doses ranging from 4,000 mg to over 200,000 mg in a 24-hour period, he commented that there was "a remarkable lack of systemic difficulties" with these doses of vitamin C. By 1993, Cathcart's patient count had exceeded 20,000, and no remarkable difficulties with these dosage levels had emerged (Cathcart, 1993). Some of his AIDS patients (Cathcart, 1984) would take anywhere from 25,000 to 125,000 mg of vitamin C daily on a regular basis, only varying the dose depending upon fluctuating bowel tolerance, which generally reflected the activity level of the disease. Cathcart noted that occasional minor complaints of gas, diarrhea, or acid stomach were seen more often in well patients, appearing only rarely in the "very sick" patients. He asserted that even with these high daily doses of vitamin C, he "cannot recall any patient who has been damaged by large doses of ascorbate," except for some dissolving effect on tooth enamel in a few people who swished the vitamin C in their mouths before swallowing.


    Cathcart also commented on the incidence of a few possible side effects that some authors feel may be associated with vitamin C therapy. Cathcart noted in the doses of vitamin C that he administered, oxalate kidney stones did not occur, and patients who had them previously tended not to get them again. Cathcart's extensive clinical experience directly contradicts the widespread but mistaken belief that large doses of vitamin C will result in kidney stone formation. Cathcart also noted that "three out of thousands" developed a "light rash" that cleared without discontinuing the vitamin C. Regarding the urinary tract, he noted that "six patients have had mild pain on urination," but that "acute and chronic urinary tract infections" were often eradicated with the vitamin C. A few patients had "discoloration of the skin" under some types of jewelry, possibly because of a detoxification effect of the vitamin C. Cathcart reported that a few patients had small sores in their mouth on lower doses of vitamin C that subsequently cleared when dosing was increased to the bowel tolerance levels. He noted that a few patients with "hidden peptic ulcers" might have had pain, but that others were benefited. Cathcart also commented that he has seen only benefit and no aggravation of gouty arthritis with high doses of vitamin C.


    Moertel et al. (1985) conducted a prospective, double-blind study of the effects of 10,000 mg vitamin C daily versus placebo on 100 patients with advanced colorectal cancer. Except for a few patients having slightly more heartburn with vitamin C than placebo (a difference the authors determined to be "not statistically significant"), no "clear evidence of a specific toxicity of vitamin C" was detected in any of the patients. However, ascorbic acid was likely the form of vitamin C administered. Had the vitamin C been given as sodium ascorbate, no heartburn at all would be anticipated. The median time of vitamin C administration was 2.5 months, with the longest duration being 15.6 months. Even though the subjects were sick patients who would be expected to be especially sensitive to any agent with even mild toxicity, the daily 10,000 mg dose was very well-tolerated with no significant side effects observed. Earlier, Creagan et al. (1979) had administered either 10,000 mg daily of vitamin C as ascorbic acid or placebo to 123 advanced cancer patients who were felt to be "unsuitable" for chemotherapy. These patients were very ill, with a median survival time of seven weeks. Nevertheless, the vitamin C was very well-tolerated, producing only mild nausea and vomiting with the same frequency as the lactose placebo pills. The authors also specifically noted that no kidney stones were produced by this therapy, even though some patients received the vitamin C for over six months.


    Bendich and Langseth (1995) compiled a good review article that also addressed the safety of chronic vitamin C supplementation. In addition to the reports noted above, a host of other therapeutic trials with vitamin C have also reported no adverse effects with dosages of vitamin C considered by most researchers and clinicians to be in the "mega-dose" range. In five double-blind studies giving either vitamin C or placebo, the doses of vitamin C ranged from 400 to 4,000 mg daily, and the durations of therapy ranged from one to 24 months (Ludvigsson et al., 1979; Bussey et al., 1982; McKeown-Eyssen et al., 1988; Taylor et al., 1991; Osilesi et al., 1991). In six other clinical trials that were not double-blinded and had no placebo given, long-term vitamin C administration did not result in any side effects. The vitamin C doses ranged from 500 to 5,000 mg daily, and the durations of therapy ranged from one to 30 months (Lux and May, 1983; Melethil et al., 1986; Brox et al., 1988; Godeau and Bierling, 1990; Reaven et al., 1993; Sharma and Mathur, 1995). In an article reviewing a large number of vitamin C studies, Hanck (1982) also confirmed the remarkable safety of long-term supplementation. Bass et al. (1998), in a double-blind study, found that vitamin C administration was very safe even for premature infants.


    It can certainly be concluded that vitamin C is an exceptionally safe supplement, which has already been given in very large doses for extended periods of time with no significant problems occurring. There are few, if any, prescription or non-prescription medicines or supplements that are as free of side effects as vitamin C. This is in spite of the fact that vitamin C has one of the widest flexibilities in dose amount of any ingestible substance. The mild gastrointestinal effect of slight heartburn or stomach upset is limited to the ascorbic acid form of vitamin C. Vitamin C is equally effective in its sodium ascorbate form, and there is no stomach upset with this preparation.


    Does Vitamin C Cause Kidney Stones?


    Vitamin C as ascorbic acid is first metabolized to oxidized ascorbic acid, or dehydroascorbic acid (DHAA). Whenever vitamin C first contributes two electrons to another compound while performing its major responsibility as an antioxidant, DHAA is immediately produced. Other antioxidants and some enzymes can promptly regenerate DHAA back to the potent, unoxidized ascorbic acid (Long and Carson, 1961; Basu et al., 1979; Rose and Bode, 1992; Bode et al., 1993). However, when this regeneration does not occur, further metabolic breakdown of vitamin C can take place. The primary metabolic pathway of vitamin C is as follows (Davies et al., 1991):

    1. Vitamin C (ascorbic acid) to DHAA
    2. DHAA to diketogulonic acid
    3. Diketogulonic acid to lyxonic acid, xylose, threonic acid, or oxalic acid (oxalate)

    Oxalate, or oxalic acid, is a major metabolite of vitamin C after it is utilized and fully broken down in the body. Oxalate is considered a true metabolic "end product" because there is no evidence that mammalian tissues further utilize it or break it down any further (Hagler and Herman, 1973). Since the primary constituent in most kidney stones is calcium oxalate (Jayanthi et al., 1994), many conventional doctors have simply concluded that significant vitamin C supplementation will lead to kidney stones. For this reason alone, it would seem that many patients are still warned by their physicians that vitamin C supplementation "might" cause problems and increase their chance of developing a kidney stone. However, there exists a large amount of literature from respected research centers that indicates otherwise. In patients with known kidney disease, some reasonable cautions are in order. However, a healthy person who avoids dehydration and ingests even very large amounts of vitamin C does not need to have any concern about kidney stone formation. In fact, there is a strong suggestion in some studies that regular supplementation of vitamin C actually decreases the chances of kidney stone development. Two recent and extensive studies at Harvard have clearly demonstrated that vitamin C is not a factor in the development of kidney stones in healthy adults. Curhan et al. (1999) looked at a group of 85,557 women with no history of kidney stones. Over a follow-up period of 14 years, 1,078 cases of kidney stones developed in this group. Vitamin C intake had no statistical association with any increased risk of stone development. A bit earlier, Curhan et al. (1996) looked at a group of 45,251 men with no history of kidney stones. They also found that vitamin C was not a risk factor for stone formation over their six years of follow-up, and it did not matter whether the men were consuming 250 mg or 1,500 mg of vitamin C daily. Gerster (1997) noted that a statistical study revealed that individuals with the highest vitamin C intake actually had a lower risk of kidney stones compared to individuals taking the least vitamin C. Analyzing the relationship more precisely, Simon and Hudes (1999) found that every 1.0 mg/dL increase in blood vitamin C levels was "independently associated" with approximately a 28% decrease in the prevalence of kidney stones in men. Gaker and Butcher (1986) reported that an 81-year-old woman successfully dissolved her very large kidney stone over an eight-week period with only diuretics, antibiotics, and vitamin C.


    In veterinary work, Belfield and Zucker (1993) reported two cases in which vitamin C administration dissolved documented bladder stones. A 10-year-old female terrier was found to have bladder stones. Since the owner did not want an operation for only that reason, the dog was placed on 500 mg of vitamin C daily. After six months the animal had unrelated uterine surgery, and an operative examination of the bladder revealed that the stones were gone. In another case, a veterinarian gave a small-breed dog 8,000 mg of vitamin C as ascorbic acid daily for four months. This successfully dissolved a large bladder stone.
    Many factors are involved in the precipitation of calcium oxalate out of the urine, leading to stone formation, and increased vitamin C supplementation is but one of these factors. It is important to realize that a given risk factor can only produce a given medical condition when other surrounding circumstances favor the development of that condition as well. These risk factors, with appropriate references, include the following:

    1. Increased urinary oxalate (Hagler and Herman, 1973b; Ogawa et al., 2000)
    2. Increased vitamin C supplementation (Pru et al., 1985; Urivetzky et al., 1992; Auer et al., 1998)
    3. Calcium ascorbate as the type of supplemental vitamin C (Kalokerinos et al., 1981; Tsugawa et al., 1999)
    4. Presence and concentration of other dissolved substances (solutes) in the urine (Oke, 1969; Lawton et al., 1985)
    5. Presence of heavy metal chelation agents, such as DMPS, DMSA, and EDTA, which have their own independent kidney toxicities, due to increased urinary solute load and toxin damage to the kidneys (Oke, 1969)
    6. Increased urinary calcium (Noe, 2000; Kinder et al., 2002; Bushinsky et al., 2002; Borghi et al., 2002)
    7. Decreased urinary magnesium (Schwartz et al., 2001)
    8. Decreased urinary citrate (Alvarez et al., 1992; Tekin et al., 2000; Yagisawa et al., 2001)
    9. Decreased urinary potassium (Kinder et al., 2002)
    10. Increased urinary cystine (Martins et al., 2002)
    11. Increased urinary phosphorus (Prie et al., 2001)
    12. Increased urinary uric acid (Koide, 1996; Yagisawa et al., 1999)
    13. Increased urinary lipids and cholesterol (Khan et al., 1988; Khan and Glenton, 1996)
    14. Increased age, with age-associated decrease in glomerular filtration rate (Mousson et al., 1993)
    15. Intake of hard water (Bellizzi et al., 1999)
    16. Overall state of hydration (Sakhaee et al., 1987; Borghi et al., 1996)
    17. Decreased daily volume of urine flow and formation (Riobo et al., 1998; Borghi et al., 1999a)
    18. Urinary pH (Wall and Tiselius, 1990; Hokama et al., 2000; Murayama et al., 2001; Kinder et al, 2002; Hsu et al., 2002)
    19. Low dietary calcium (Curhan et al., 1997a)
    20. Supplemental calcium (Curhan et al., 1997a); supplemental calcium causing calcium gallstones (Powell, 1985)
    21. Vitamin D supplementation (Black, 1945; Hodgkinson and Zarembski, 1968; Broadus et al., 1980; Ichioka et al., 2002)
    22. Low intake of magnesium and vitamins (Williams and Smith, 1968)
    23. Preexisting calcium deposits throughout the body, especially in the vascular system
    24. Presence of preexisting kidney insufficiency or failure; being on hemodialysis (Oren et al., 1984; Chen et al., 1990; Daudon et al., 1992)
    25. Any injury to the cells lining those parts of the urinary system susceptible to stone formation (Khan and Thamilselvan, 2000)
    26. Intake of oxalate stone-generating or oxalate-containing foods (Hagler and Herman, 1973a; Bakane et al., 1999; Massey et al., 2001)
    27. Intake of oxalate stone-generating or oxalate-containing beverages (McKay et al., 1995; Curhan et al., 1996a; Terris et al., 2001)
    28. Intake of oxalate stone-generating or oxalate-containing supplements and medicines (Shields and Simmons, 1976; Fleisch, 1978; Ettinger et al., 1980; Wolf et al., 1985; Ahlstrand and Tiselius, 1987; Daudon et al., 1987; Michelacci et al., 1992; Kohan et al., 1999; Sundaram and Saltzman, 1999; Gonzalez et al., 2000; Wu and Stoller, 2000)
    29. Intake of oxalate stone-generating toxins (Hagler and Herman, 1973c; Conyers et al., 1990; Muthukumar and Selvam, 1998)
    30. Receiving total parenteral nutrition (Friedman et al., 1983; Swartz et al., 1984)
    31. Deficiency of pyridoxine [vitamin B6] (Gershoff et al., 1959; Faber et al., 1963; Gershoff, 1964; Mitwalli et al., 1988; Alkhunaizi and Chan, 1996; Curhan et al., 1999)
    32. Deficiency of thiamine [vitamin B1] (Buckle, 1963; Alkhunaizi and Chan, 1996)
    33. Having had intestinal bypass or resection surgery, or small bowel malabsorption from any cause (Gregory et al., 1977; Drenick et al., 1978; Nightingale, 1999; Nightingale, 2001)
    34. Urinary tract infection, or presence of bacteria (Trinchieri et al., 1996; Dewan et al., 1997; Daskalova et al., 1998; Hokama et al., 2000; Sohshang et al., 2000; Kim et al., 2001)
    35. Presence of increased oxidative stress in the urinary tract (Scheid et al., 1996; Muthukumar and Selvam, 1998)
    36. Primary hyperoxaluria, a hereditary disorder (Daudon et al., 1998)
    37. Hyperparathyroidism (Ralph-Edwards et al., 1992; Yamaguchi et al., 2001)
    38. Urinary stasis, or incomplete voiding (Nikakhtar et al., 1981; Sarkissian et al., 2001)
    39. Obstructive urinary disease (Kim et al., 2001)
    40. Polycystic kidney disease (Torres et al., 1988; Torres et al., 1993)
    41. Cirrhosis (Hagler and Herman, 1973c)
    42. Diabetes (Hagler and Herman, 1973c)
    43. Congestive heart failure (Hagler and Herman, 1973c)
    44. Crohn's disease (Shiraishi et al., 1998; Buno et al., 2001; McConnell et al., 2002)
    45. Cystic fibrosis (Turner et al., 2000; Perez-Brayfield et al., 2002)
    46. Renal tubular acidosis (Hagler and Herman, 1973c)
    47. Sarcoidosis (Sharma, 1996; Rodman and Mahler, 2000)
    48. Klinefelter's syndrome (Hagler and Herman, 1973c)
    49. Parasitic diseases, including amebiasis, schistosomiasis, giardiasis, and ascariasis (Hagler and Herman, 1973c)
    50. Antibiotic therapy (Bohles et al., 2002)
    51. Increased fluoride intake (Singh et al., 2001)
    52. Prolonged bedrest (Hwang et al., 1988)
    53. Kidney transplantation (Torrecilla et al., 2001)
    54. Hypertension (Borghi et al., 1999; Hall et al., 2001)
    55. Increased alcohol intake (Hughes and Norman, 1992)
    56. Increased glucose intake (Burns et al., 1951; Nguyen et al., 1989)
    57. Pregnancy (Hildebrandt and Shanklin, 1962; Maikranz et al., 1989)
    58. Methoxyflurane anesthesia (Mazze et al., 1971; Mazze et al., 1971a; Silverberg et al., 1971)
    59. Ketogenic diet (Furth et al., 2000)
    60. Space travel (Whitson et al., 1997; Whitson et al., 1999)

    One of the primary reasons why the vitamin C/kidney stone connection continues to generate concern is because vitamin C does increase the urinary concentration of oxalate. Therefore, it just seems logical to assume that more and prolonged vitamin C administration will continue to increase this concentration until calcium oxalate stones begin to form. However, research proves that this is not the case, although vitamin C is one of many risk factors (see above) for increased oxalate formation and the subsequent formation of calcium oxalate stones. Schmidt et al. (1981) determined that there was actually a leveling off of oxalate production even though the vitamin C dosing was continued. The researchers noted that a significant amount of the vitamin C does not even get metabolized to oxalate and is excreted unchanged in the urine. When very high doses of vitamin C are administered for any significant medical condition, the active, non-oxidized form of vitamin C is much more readily regenerated from the oxidized vitamin C that is initially generated. This process further prevents the irreversible metabolism of vitamin C to the oxalate end product. Takenouchi et al. (1966) noted that about 80% of vitamin C administered to human subjects was eliminated as dehydroascorbic acid, the oxidized form of vitamin C. They concluded that the metabolic breakdown of vitamin C in humans does not necessarily have to follow the entire sequence down to oxalate. They also noted that as the vitamin C dose is increased, urinary excretion of diketogulonic acid increased. This is a clear indication that further oxidative breakdown of the diketogulonic acid to oxalate does not have to occur for a metabolic breakdown product of vitamin C to be excreted. In healthy men, Lamden and Chrystowski (1954) showed that vitamin C doses of 4,000 mg or less "produced no significant increase in oxalate excretion" over non-supplementers. Fituri et al. (1983) found that the ingestion of 8,000 mg of vitamin C daily for seven days by eight normal subjects did not "significantly alter urinary or plasma oxalate during or after ingestion." Other investigators have found that vitamin C administration will raise urinary oxalate levels (Tiselius and Almgard, 1977; Hatch et al., 1980; Hughes et al, 1981). As noted in the list above, vitamin C is only one of many risk factors that can affect whether calcium oxalate stones are ultimately formed. Unfortunately, many of the research studies examining this issue have not even looked for most of the other risk factors itemized above, resulting in conflicting findings on the ability of vitamin C to increase urinary oxalate. Fituri et al. even noted that some studies have used a tablet form of vitamin C, and they suggested that the tartaric acid and sucrose present in some tablets could convert to oxalate in the body. The amounts of such additional agents in pills can be significant, as Wilk (1976) noted that 100 mg vitamin C pills weighed 400 mg, with the additional 300 mg due to fillers. Auer et al. (1998a) also showed that urine specimens not preserved with EDTA registered erroneously high oxalate levels in their testing, possibly indicating a reason for some of the higher oxalate levels noted in other urine studies of vitamin C supplementers.


    Logically, there have to be multiple other ways to metabolize and excrete vitamin C rather than by urinary oxalate. Casciari et al., (2001) showed that 50,000 mg daily doses of intravenous vitamin C have already been given to cancer patients for eight-week periods without problem. If urinary oxalate was the only excreted metabolic product of vitamin C, such doses would cause such a supersaturation of oxalate in the urine that crystal deposition and eventual stone formation would have to occur. Yet, this does not occur.
    Since oxalate is a primary component of so many kidney stones, it is also very important to know about the many other potential sources of increased oxalate concentration in the urine. In addition to vitamin C, glyoxylate and glycolate are the primary substances that can be metabolized to oxalate (Ogawa et al., 2000). Also, there are numerous other lesser precursors to oxalate, including gelatin, certain amino acids (such as tryptophan, phenylalanine, aspartic acid, tyrosine, threonine, and asparagine), creatinine, purines, glucose, other carbohydrates, and probably several unidentified substances (Hagler and Herman, 1973). A lesser precursor can assume a great deal of importance in the generation of oxalate when one has a peculiar diet rich in the precursor, such as occurs in the regular excessive ingestion of aspartame-containing diet drinks and other diet foods. Aspartame is primarily a combination of phenylalanine and aspartic acid, two of the amino acids that can lead to oxalate. Also, if a patient is receiving hyperalimentation with a high concentration of amino acids, increased oxalate formation can result. Glycine, the simplest of the amino acids, is likely the major source of glyoxylate, which is a major immediate precursor to oxalate (Hagler and Herman, 1973).


    Important dietary sources of oxalate include spinach, rhubarb, parsley, citrus fruits, and tea. Tea is probably the most important source of oxalate in the average English diet (Zarembski and Hodgkinson, 1962). Other significant dietary sources of oxalate include Swiss chard, cocoa, chocolate, beet tops, peppers, wheat germ, pecans, peanuts, okra, chocolate, refried beans, lentils, and lime peel. Various soy-based foods can also contain large amounts of oxalate (Massey et al., 2001). High-purine foods, such as sardines and herring roes, also substantially increase oxalate excretion (Zarembski and Hodgkinson, 1969). Oxalate poisoning has been reported in the literature secondary to an excessive intake of rhubarb (Tallquist and Vaananen, 1960; Kalliala and Kauste, 1964). Clearly, a detailed dietary history is critical in the proper management of any patient with kidney stone risk or disease, and merely lessening or discontinuing vitamin C intake as the only significant intervention is not in the patient's best interests. Eliminating one or several of the patient's favorite oxalate-containing foods should always take precedence over lessening or eliminating any regular supplementation of vitamin C.


    Calcium also plays several roles in the propensity for calcium oxalate stone formation. Reducing the dietary (not supplemental) intake of calcium increases the intestinal absorption of oxalate (Hodgkinson, 1958). Conversely, in a study on 45,619 men Curhan et al. (1993) found that a high dietary intake of calcium decreased the risk of symptomatic kidney stones. In looking at 91,731 women, Curhan et al. (1997) again found that the high dietary intake of calcium decreased the risk of symptomatic kidney stones, "whereas intake of supplemental calcium may increase risk." It was also found that vitamin D supplementation increased the excretion of oxalate in humans (Hodgkinson and Zarembski, 1968).
    Some researchers have actually demonstrated that vitamin C probably lessens the likelihood of kidney stone formation in those individuals who already have a history of stone formation, indicating a possible therapeutic role for vitamin C in the treatment of kidney stone disease. Schwille et al. (2000) found that vitamin C actually inhibited the development of calcium oxalate crystals in these individuals. Not surprisingly, they also concluded that vitamin C does not play a role in helping the formation of kidney stones "under normal conditions." Grases et al. (1998) were able to demonstrate that free radical-damaged cells in an experimental model using living epithelial cells tended to produce a "favorable environment" for the development of calcium oxalate crystals. They found the vitamin C "exerted the most remarkable effects" in preventing the formation of calcium oxalate crystals. Selvam (2002) found that "antioxidant therapy prevented calcium oxalate precipitation in the rat kidney and reduced oxalate excretion in stone patients." Gotz et al. (1986) showed that another antioxidant, lipoic acid, helped prevent the precipitation of calcium oxalate crystals in dogs. Jayanthi et al. (1994) also showed that lipoic acid was effective in lowering oxalate levels in the kidneys and urine of rats. As a powerful antioxidant, vitamin C may well have the same effects as lipoic acid. Certainly, vitamin C also quenches free radicals, prevents oxidant-induced damage, and facilitates tissue healing after such damage has been inflicted. Perhaps eliminating focal areas of such tissue damage makes it that much more difficult to initiate an abnormal deposit of calcium oxalate. This may be one significant way in which vitamin C can reduce kidney stone formation. McCormick (1946) long ago asserted that his research on vitamin C indicated that a vitamin C deficiency was "the basic etiological factor" for stone formation anywhere in the body.

  33. #153
    Kärnfysikern's Avatar
    Kärnfysikern is offline Retired: AR-Hall of Famer
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    by the way you asked about lysin if we get enough. 100grams of whey concetrat contains 8grams of lysin. I dont know anout meat though. But looks like we bodybuilders should have plenty of lysin

    Maby if eating pure lysin like on a empty stomach it gets absorbed better into the bloodstream? But I get around 16 grams of lysin daily from my shakes if not even upp to 24grams so I dont worry

  34. #154
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    Alpha-Male is offline Senior Member
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    sorry, been out all day, finished up my two root canals and prepped for crowns...OUCH!!!

    hey bro, PLEASE try to get a copy of that book, Nutrient Timing...i'm going to work on getting it to PDF somehow...i was re-reading it earlier, and they too advocate the use of Vit. C AND E, as well as leucine in pre and post workout nutrition, for many of the reasons we've discussed...maybe i'll just try to post or send you the excerpts...i'd be interested to get some other's opinions on some of the topics discussed...peace

  35. #155
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    Kärnfysikern is offline Retired: AR-Hall of Famer
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    yeah. when I get cash I will order it or buy it on pdf I realy want to read that one for sure

  36. #156
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    Kärnfysikern is offline Retired: AR-Hall of Famer
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    hope your mouth is feeling better

  37. #157
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    Kärnfysikern is offline Retired: AR-Hall of Famer
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    feelt good in the gym. Will weight myself tomorrow but dont except any weightloss since last week since I had 2 cheat days last weekend.

    Had gained 10 ibs in a chest press and in shoulder press. Was a bit stronger then last time in close grip bench and my deadlift strenght was awsome.

  38. #158
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    IT:S GREAT WHAT U GUYS ARE POSTING BUT I DON:T THINK I HAVE TIME TO READ ALLLLL OF IT...

    anyways, can someone concluded it??? the benefits, dosage, side effects

  39. #159
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    Quote Originally Posted by Alpha-Male
    sorry, been out all day, finished up my two root canals and prepped for crowns...OUCH!!!

    hey bro, PLEASE try to get a copy of that book, Nutrient Timing...i'm going to work on getting it to PDF somehow...i was re-reading it earlier, and they too advocate the use of Vit. C AND E, as well as leucine in pre and post workout nutrition, for many of the reasons we've discussed...maybe i'll just try to post or send you the excerpts...i'd be interested to get some other's opinions on some of the topics discussed...peace
    and high GI carbs before workout..during?(cant remember) and after....it sounds intresting tho.....ill look for it too...let me know if you get it......
    Damn 2 root canals?!!!i had one from a fight that was a total bitch...good luck

  40. #160
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    well, i can't find the damn thing, checked Amazon.com, no luck...Kinko's won't do it without copyright permission, and it would cost too much and take up WAY too much time for me to do it...Barnes and Noble or Amazon.com has the paperback, it's only like $10...you should definitely order it...

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